Biomedical subjects

S Qin

Publications and source records attributed to S Qin.

At least 73 records · Page 4Linked to original sources

PubMed1999

[Nested polymerase chain reaction in detecting Mycobacterium tuberculosis DNA in bioptic tissue from patients with endobronchial tuberculosis].

OBJECTIVE: To evaluate the nested polymerase chain reaction (NPCR) technique in diagnosing endobronchial tuberculosis. METHODS: NPCR method was used to detect Mycobacterium tuberculosis DNA in bioptic tissue from 67 patients with endobronchial tuberculosis, and the results were compared with pathologic examination, brushing smear, sputum smear and culture for Mycobacterium tuberculosis after bronchoscopy. The controls were 43 patients with lung cancer. RESULTS: The positive rates of detecting Mycobacterium tuberculosis were 13%, 19%, 22%, 15% and 76% respectively by pathologic examination, brushing smear, sputum smear, culture after bronchoscopy and NPCR methods. Significant differences were found between NPCR and the other 4 methods (all Ps < 0.01). No positive result for Mycobacterium tuberculosis was found in 43 controls by NPCR. CONCLUSIONS: NPCR is a useful method for diagnosing patients with endobronchial tuberculosis, especially for those with normal demonstration in X-ray chest film, negative sputum and nonspecific pathologic changes in endobronchial biopsy.

Biopsy↗

PubMed1999

[Morphological cure of cerebral arteriovenous malformations by endovascular therapeutics].

OBJECTIVE: To sum up the clinical characteristics and typical manifestation by analysing clinical materials from total embolized cerebral arteriovenous malformations (AVM) via endovascular embolization. METHODS: We reviewed clinical and image materials of 50 patients whose cerebral AVM were embolized entirely and found the cerebral AVM morphological cure by endovascular embolization after studying the size, position, artery supply, therapeutics and follow-up. RESULTS: 50 patients with cerebral AVM were embolized by endovascular therapy, accounting for 17% of all patients. Malformation lesions were medium or small type, with a diameter less than 3 cm, 95% of them were located in the tentorium superior. Terminal end blood supply was common to AVM and especially medium cerebral artery (MCA) or its branches. 97% of the patients were graded III or below by spectzler grading system. 70% of them had a history of intracranial hemorrhage and were cured by one therapy. CONCLUSIONS: It is a reliable and feasible method for morphological cure in cerebral AVM via endovascular therapeutics only, but case selection is important, that is, medium or small AVM with single branch terminal end blood supply in the tentorium superior.

Adolescent↗

PubMed1999

[Survey on traditional medicinal resources of Uncaria distributed in China].

OBJECTIVE: To make clear the botanical origin of medicinal Uncaria distributed in China and the situation of its use in folk medicines. METHODS: Collecting data and making on-the-spot investigation. RESULTS: There are thirteen medicinal plants which belong to Uncaria genus, and ten of them are commercially available. A clear idea was obtained of their geographical distribution, distribution features and practical experiences in folk application. CONCLUSION: This investigation is helpful in further researching and exploring the resources of Uncaria for medical use, as well as provides a scientific basis for production, management and safe use of crude drugs.

China↗

PubMed1999

[HBsAg expression, anti-HBs induction and pathological observation in the mice inoculated with DNA vaccine against hepatitis B].

OBJECTIVE: To study if special humoral immunological response can be induced by DNA vaccine against Hepatitis B (NV-HB/s) and its mechanism. METHODS: The Balb/C mice inoculated with NV-HB/s by intramuscular injection were detected for HBsAg(the expressed product of NV-HB/s) by ABC immunohistochemistry or ELISA, and for anti-HBs by ELISA and also performed the routine pathological examination. RESULTS: After inoculated with NV-HB/s, HBsAg could be detected from mice muscle tissue samples of injected sites one week later and almost kept positive(75% and even more) up to 6th month, but was undetectable from all the serum samples during this period; anti-HBs could be detected from serum samples of some mice two weeks later and of all the mice detected one month later, it still kept positive at 6th month while the mice were sacrificed. Under microscope, only non-specific inflammation was found in the muscle tissues of injected sites and could completely recover within 4 weeks, no matter whether the mice were inoculated with NV-HBs, or with traditional HB vaccine derived from blood, or even with PBS as control. CONCLUSION: DNA vaccine against Hepatitis B (NV-HB/s) can successfully express HBsAg in the muscle tissue of mice by intramuscular inoculation and subsequently induce anti-HBs in vitro.

Animals↗

PubMed1998

Involvement of the IP-10 chemokine in sarcoid granulomatous reactions.

The accumulation of T cells and monocytes at sites of ongoing inflammation represents the earliest step in the series of events that lead to granuloma formation in sarcoidosis. In this study, we evaluated the pulmonary production of IFN-inducible protein 10 (IP-10), a CXC chemokine that stimulates the directional migration of activated T cells. Striking levels of IP-10 were demonstrated in the bronchoalveolar lavage (BAL) fluid of 24 patients with pulmonary sarcoidosis and lymphocytic alveolitis, as compared with patients with inactive disease or control subjects. A positive correlation was demonstrated between IP-10 levels and the number of sarcoid CD45R0+/CD4+ cells in the BAL. Immunochemistry, performed with an anti-human IP-10 polyclonal Ab in lymph nodes displaying prominent sarcoid granulomas, showed that cells bearing IP-10 were mainly epithelioid cells and CD68+ macrophages located inside granulomatous areas. Macrophages recovered from the BAL of sarcoid patients stained positive for IP-10 protein. Furthermore, alveolar macrophages isolated from sarcoid patients with T cell alveolitis and cultured for 24 h in presence of IFN-gamma secreted definite levels of IP-10 capable of inducing T cell chemiotaxis. Interestingly, alveolar lymphocytes recovered from patients with active sarcoidosis were CD4+ T cells expressing Th1 cytokines (IL-2 and IFN-gamma) and high levels of CXCR3. Taken together, these data suggest the potential role of IP-10 in regulating the migration and activation of T cells toward sites of sarcoid inflammatory process and the consequent granuloma formation.

Adult↗

PubMed1998

The alpha-chemokine, stromal cell-derived factor-1alpha, binds to the transmembrane G-protein-coupled CXCR-4 receptor and activates multiple signal transduction pathways.

The alpha-chemokine stromal cell-derived factor (SDF)-1alpha binds to the seven transmembrane G-protein-coupled CXCR-4 receptor and acts to modulate cell migration and proliferation. The signaling pathways that mediate the effects of SDF-1alpha are not well characterized. We studied events following SDF-1alpha binding to CXCR-4 in a model murine pre-B cell line transfected with human CXCR-4. There was enhanced tyrosine phosphorylation and association of components of focal adhesion complexes such as the related adhesion focal tyrosine kinase, paxillin, and Crk. We also observed activation of phosphatidylinositol 3-kinase. Wortmannin, a selective inhibitor of phosphatidylinositol 3-kinase, partially inhibited the SDF-1alpha-induced migration and tyrosine phosphorylation of paxillin. SDF-1alpha treatment selectively activated p44/42 mitogen-activated protein kinase (Erk 1 and Erk 2) and its upstream kinase mitogen-activated protein kinase kinase but not p38 mitogen-activated protein kinase, c-Jun amino-terminal kinase or mitogen activated protein kinase kinase. We also observed that SDF-1alpha treatment increased NF-kappaB activity in nuclear extracts from the CXCR-4 transfectants. Taken together, these studies revealed that SDF-1alpha activates distinct signaling pathways that may mediate cell growth, migration, and transcriptional activation.

Animals↗

PubMed1998

A deficiency in Syk enhances ceramide-induced apoptosis in DT40 lymphoma B cells.

Syk deficiency significantly enhanced ceramide-induced apoptosis. Ectopic expression of wild-type or kinase-inactive Syk rendered Syk-negative cells resistant to ceramide-induced apoptosis. Furthermore, ceramide could not activate Syk, indicating that Syk protected DT40 cells from ceramide-induced apoptosis, via a mechanism independent of its activity. In addition, a deficiency in Lyn also resulted in the cells becoming susceptible to ceramide-induced apoptosis. However, no difference of Ara-C-induced apoptosis between wild-type and mutant cells was observed. c-Jun N-terminal kinases appeared not to be important in mediating the enhanced apoptosis, as they were still activated in mutant cells following ceramide treatment.

Apoptosis↗

PubMed1998

Differential regulation of oxidative and osmotic stress induced Syk activation by both autophosphorylation and SH2 domains.

Syk, a nonreceptor protein-tyrosine kinase, is activated by both oxidative and osmotic stress and plays different roles in the transduction of stress signals. In this study, the regulation of oxidative and osmotic stress induced Syk activation was investigated utilizing Syk-negative DT40 cells, expressing various Syk mutants. Phosphorylation of Y518Y519 was demonstrated to be required for both oxidative and osmotic stress induced Syk activation. Syk activation by these two types of stress stimuli was a combination of both autophosphorylation and the activities of additional tyrosine kinases. Oxidative stress induced Syk tyrosine phosphorylation was almost completely attributed to autophosphorylation, whereas other tyrosine kinases were largely responsible for osmotic stress induced Syk tyrosine phosphorylation. Moreover, the Src homology 2 (SH2) domains of Syk differentially regulated Syk activation. Both mSH2(N) Syk and mSH2(C) Syk, in which the phosphotyrosine-dependent binding motif within the SH2 domains contained point mutations, showed a significantly higher activity than that observed in wild-type Syk, following osmotic stress treatment. In comparison, in response to oxidative stress, only mSH2(N) Syk demonstrated a stronger activation than wild-type Syk. Therefore, differential activation and regulation of Syk may give an insight into the distinctive functions of Syk in oxidative and osmotic stress signaling.

Animals↗

PubMed1998

The chemokine receptors CXCR3 and CCR5 mark subsets of T cells associated with certain inflammatory reactions.

T cells infiltrating inflammatory sites are usually of the activated/memory type. The precise mechanism for the positioning of these cells within tissues is unclear. Adhesion molecules certainly play a role; however, the intricate control of cell migration appears to be mediated by numerous chemokines and their receptors. Particularly important chemokines for activated/memory T cells are the CXCR3 ligands IP-10 and Mig and the CCR5 ligands RANTES, macrophage inflammatory protein-1alpha, and macrophage inflammatory protein-1beta. We raised anti-CXCR3 mAbs and were able to detect high levels of CXCR3 expression on activated T cells. Surprisingly, a proportion of circulating blood T cells, B cells, and natural killer cells also expressed CXCR3. CCR5 showed a similar expression pattern as CXCR3, but was expressed on fewer circulating T cells. Blood T cells expressing CXCR3 (and CCR5) were mostly CD45RO+, and generally expressed high levels of beta1 integrins. This phenotype resembled that of T cells infiltrating inflammatory lesions. Immunostaining of T cells in rheumatoid arthritis synovial fluid confirmed that virtually all such T cells expressed CXCR3 and approximately 80% expressed CCR5, representing high enrichment over levels of CXCR3+ and CCR5+ T cells in blood, 35 and 15%, respectively. Analysis by immunohistochemistry of various inflamed tissues gave comparable findings in that virtually all T cells within the lesions expressed CXCR3, particularly in perivascular regions, whereas far fewer T cells within normal lymph nodes expressed CXCR3 or CCR5. These results demonstrate that the chemokine receptor CXCR3 and CCR5 are markers for T cells associated with certain inflammatory reactions, particularly TH-1 type reactions. Moreover, CXCR3 and CCR5 appear to identify subsets of T cells in blood with a predilection for homing to these sites.

Animals↗

PubMed1998

Rapid and coordinated switch in chemokine receptor expression during dendritic cell maturation.

Dendritic cells (DC) migrate into inflamed peripheral tissues where they capture antigens and, following maturation, to lymph nodes where they stimulate T cells. To gain insight into this process we compared chemokine receptor expression in immature and mature DC. Immature DC expressed CCR1, CCR2, CCR5 and CXCR1 and responded to their respective ligands, which are chemokines produced at inflammatory sites. Following stimulation with LPS or TNF-alpha maturing DC expressed high levels of CCR7 mRNA and acquired responsiveness to the CCR7 ligand EBI1 ligand chemokine (ELC), a chemokine produced in lymphoid organs. Maturation also resulted in up-regulation of CXCR4 and down-regulation of CXCR1 mRNA, while CCR1 and CCR5 mRNA were only marginally affected for up to 40 h. However, CCR1 and CCR5 were lost from the cell surface within 3 h, due to receptor down-regulation mediated by chemokines produced by maturing DC. A complete down-regulation of CCR1 and CCR5 mRNA was observed only after stimulation with CD40 ligand of DC induced to mature by LPS treatment. These different patterns of chemokine receptors are consistent with "inflammatory" and "primary response" phases of DC function.

Cell Differentiation↗

PubMed1998

The bipartite geminivirus coat protein aids BR1 function in viral movement by affecting the accumulation of viral single-stranded DNA.

The movement of bipartite geminiviruses such as squash leaf curl virus (SqLCV) requires the cooperative interaction of two essential virus-encoded movement proteins, BR1 and BL1. While the viral coat protein AR1 is not essential for systemic infection, genetic studies demonstrate that its presence masks the defective phenotype of certain BR1 missense mutants, thus suggesting that coat protein does interact with the viral movement pathway. To further examine the mechanism of this interaction, we have constructed alanine-scanning mutants of AR1 and studied them for the ability to mask the infectivity defects of appropriate BR1 mutants, for the ability to target to the nucleus and to bind viral single-stranded DNA (ssDNA) and multimerize, and for effects on the accumulation of replicated viral ssDNA. We identified a specific region of AR1 required for masking of appropriate BR1 mutants and showed that this same region of AR1 was also important for ssDNA binding and the accumulation of viral replicated ssDNA. This region of AR1 also overlapped that involved in multimerization of the coat protein. We also found that the accumulation in protoplasts of single-stranded forms of a recombinant plasmid that included the SqLCV replication origin but was too large to be encapsidated was dependent on the presence of AR1 but did not appear to require encapsidation. These findings extend our model for SqLCV movement, demonstrating that coat protein affects viral movement through its ability to induce the accumulation of replicated viral ssDNA genomes. They further suggested that encapsidation was not required for the AR1-dependent accumulation of viral ssDNA.

Amino Acid Sequence↗

PubMed1998

[Clinical value of a rapid immunochromatographic assay in diagnosis and differential diagnosis of bone and joint tuberculosis].

OBJECTIVE: To evaluate the clinical value of a rapid immunochromatographic assay in diagnosis and differential diagnosis of bone and joint tuberculosis. METHOD: Antibodies in sera from 75 patients with active bone and joint tuberculosis, 69 patients with non-tuberculous bone and joint diseases and 72 healthy individuals were detected by the rapid immunochromatographic assay using ICT-TB kit. RESULT: The positive rate was found to be 80% in the patients with active bone and joint tuberculosis, while 90% in the group with spinal tuberculosis, 53% in the extra-spinal articular tuberculosis. The false positive rates were 4% and 3% respectively in those with other bone and joint diseases and healthy individuals. CONCLUSION: The assay is a rapid, sensitive and specific supplementary tool for the diagnosis of the bone and joint tuberculosis.

Antibodies, Bacterial↗

PubMed1998

[Effects of heat, noise, and their combination on plasma atrial natriuretic peptides, cardiodilatin, endogenous digitalis like substance, angiotensin II and endothelin in rats].

Plasma contents of atrial natriuretic peptides (ANP), cardiodilatin (CDD), endogenous digitalis like substance (EDLS), angiotensin II (A II) and endothelin (ET) were determined in rats following exposure to high temperature, noise and a combination of the two. It was found that plasma content of ANP after heat exposure decreased significantly, CDD and A II content after heat or noise exposure increased obviously, ET content decreased significantly after exposure to combined factors. ANP and CDD have the same physiological function and changes. ANP, CDD and A II observed in the present study were considered to be compensatory responses. It is harmful if exposure to high temperature or noise lasts for a long time.

Angiotensin II↗

PubMed1998

[A survey on botanical origins of drug tiannanxing produced in Sichuan].

According to the investigation and identification of botanical origins of 7 species and 1 variety of the traditional Chinese drug Tiannanxing produced in Sichuan, it has been found out that the main species available on the market are Arisaema erubescens and A. heterophyllum, while A. asperatum, A. wilsonii and A. fargesil come second. A key for their identification is presented in this paper.

China↗

PubMed1997

Up-regulation of Syk activity during HL60 cell differentiation into granulocyte but not into monocyte/macrophage-lineage.

Following induction of cell differentiation in vitro, an increase in Syk activity was observed only in HL60 cells differentiation into granulocytes induced by all trans retinoic acid (RA) but not into macrophages induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) or monocytes induced by sodium butyrate. This elevation of Syk activity was the specific increase in kinase activity because the Syk amount was not altered before and after differentiation. Anti-phosphotyrosine blot revealed that tyrosine phosphorylation of Syk was significantly increased as the function of induction time by RA, but not by TPA and sodium butyrate, suggesting that tyrosine phosphorylation might account for Syk activation. More importantly, Syk tyrosine phosphorylation and Syk activity were not altered in U937 and K562 cells which undergo monocyte differentiation and no differentiation, respectively, in response to RA induction. Taken together, Syk might exert a unique role in directing HL60 cells toward granulocyte differentiation.

Butyrates↗

PubMed1997

Distinctive functions of Syk and Lyn in mediating osmotic stress- and ultraviolet C irradiation-induced apoptosis in chicken B cells.

By taking advantage of the established chicken B cell line, DT40 cells, which do not express tyrosine kinase Syk or Lyn, functional roles of Syk and Lyn in apoptotic response elicited by cellular stress were investigated. DT40 cells underwent apoptosis after hyperosmotic stress. In Syk-deficient DT40 cells, this apoptotic process was significantly enhanced. Ectopic expression of wild type, but not kinase-inactive, porcine Syk in Syk-deficient cells rescued cells from osmotic stress-induced apoptosis, demonstrating that the presence of functionally active Syk is necessary to protect cells from osmotic stress-induced apoptosis. In comparison, there was no effect on osmotic stress-induced apoptosis in Lyn-deficient DT40 cells. Interestingly, while Syk was not involved in ultraviolet C (UVC)-induced apoptosis, a deficiency of Lyn rendered cells resistant to UVC irradiation. These observations defined Syk and Lyn as important mediators of apoptosis in DT40 cells in response to osmotic stress and UVC irradiation, respectively. Furthermore, osmotic stress, but not UVC irradiation, could activate c-Jun N-terminal kinase (JNK) in DT40 cells. A deficiency in either Syk or Lyn did not affect the osmotic stress-induced activation of JNK. We, therefore, concluded that Syk and Lyn regulate the apoptotic responses to osmotic stress and UVC irradiation independently of the JNK pathway in DT40 cells.

Animals↗

PubMed1997

Syk-dependent and -independent signaling cascades in B cells elicited by osmotic and oxidative stress.

It was found that Syk protein-tyrosine kinase is rapidly activated in B cells after H2O2 treatment (oxidative stress) or increased extracellular NaCl concentration (osmotic stress) as well as in response to B cell receptor activation. In this study we examined the involvement of Syk in responses elicited by these types of extracellular stress, particularly Ca2+ responses and c-Jun amino-terminal kinase (JNK) activation, using a chicken B cell line, DT40, as well as the DT40-derived mutant DT40/Syk(-), which does not express Syk. Osmotic stress evokes increases in [Ca2+]i by stimulating an extracellular Ca2+ influx in both DT40 and DT40/Syk(-) cells. In comparison, oxidative stress elicits an increase in [Ca2+]i by stimulating both an extracellular Ca2+ influx and Ca2+ release from internal stores in DT40 cells, but this Ca2+ response is partially abolished in DT40/Syk(-) cells, indicating that the oxidative stress-induced Ca2+ response is at least partly dependent on Syk. Interestingly, the depletion of Ca2+ results in a significantly decreased level of Syk activation in DT40 cells stimulated by oxidative but not osmotic stress. Furthermore, JNK is activated to different extents by these two types of stress. The extent of JNK activation in DT40/Syk(-) cells in response to osmotic stress is comparable to that observed in DT40 cells. Intriguingly, oxidative stress-induced JNK activation is significantly compromised in DT40/Syk(-) cells. Collectively, these results indicate that both the Ca2+ response and JNK activity induced by oxidative stress are partly dependent on Syk, whereas those induced by osmotic stress are independent of Syk.

Animals↗

PubMed1997

Chemokine receptor usage by human eosinophils. The importance of CCR3 demonstrated using an antagonistic monoclonal antibody.

Chemokines bind and signal through G-protein coupled seven transmembrane receptors. Various chemokine receptors are expressed on leukocytes, and these may impart selective homing of leukocyte subsets to sites of inflammation. Human eosinophils express the eotaxin receptor, CCR3, but respond to a variety of CC chemokines apart from eotaxin, including RANTES, monocyte chemotactic protein (MCP)-2, MCP-3, and MCP-4. Here we describe a mAb, 7B11, that is selective for CCR3 and has the properties of a true receptor antagonist. 7B11 blocked binding of various radiolabeled chemokines to either CCR3 transfectants, or eosinophils. Pretreatment of eosinophils with this mAb blocked chemotaxis and calcium flux induced by all CCR3 ligands. In all individuals examined, including allergic and eosinophilic donors, > 95% of the response of eosinophils to eotaxin, RANTES, MCP-2, MCP-3, and MCP-4 was shown to be mediated through CCR3. The IL-8 receptors, particularly CXCR2, were induced on IL-5 primed eosinophils, however these eosinophils responded to CC chemokines in the same manner as unprimed eosinophils. These results demonstrate the importance of CCR3 for eosinophil responses, and the feasibility of completely antagonizing this receptor.

Antibodies, Monoclonal↗